Analysis of the secondary structure of linker histone H1 based on IR absorption spectra

The effectiveness is compared of the infrared spectroscopy in the amide I region and UV circular dichroism to the analysis of the protein secondary structure by the example of the linker histone H1 and bovine serum albumin (BSA). It has been shown that the application of a diamond ATR cell gives the quantitative estimate of the fraction of α-helices and β-structures which are in a good agreement with UV circular dichroism spectroscopy. It has been shown that the histone H1 is able to aggregate, which results in considerable changes in its secondary structure.     

Divalent cation chelators citrate and EDTA unmask an intrinsic uncoupling pathway in isolated mitochondria

We demonstrate a suppression of ROS production and uncoupling of mitochondria by exogenous citrate in Mg²⁺ free medium. Exogenous citrate suppressed H₂O₂ emission and depolarized mitochondria. The depolarization was paralleled by the stimulation of respiration of mitochondria. The uncoupling action of citrate was independent of the presence of sodium, potassium, or chlorine ions, and it was not mediated by the changes in permeability of the inner mitochondrial membrane to solutes. The citrate transporter was not involved in the citrate effect. Inhibitory analysis data indicated that several well described mitochondria carriers and channels (ATPase, IMAC, ADP/ATP translocase, mPTP, mKATP) were not involved in citrate’s effect. Exogenous MgCl₂ strongly inhibited citrate-induced depolarization. The uncoupling effect of citrate was demonstrated in rat brain, mouse brain, mouse liver, and human melanoma cells mitochondria. We interpreted the data as an evidence to the existence of a hitherto undescribed putative inner mitochondrial membrane channel that is regulated by extramitochondrial Mg²⁺ or other divalent cations.     

Genotypic characteristics of Mycobacterium avium subsp. hominissuis strains

Mycobacterium avium are typical environmental, non-tuberculosis microorganisms that occasionally cause mycobacteriosis, an infectious disease in wild and domestic animals, birds, and humans. Here, we report the results of the first study on the genetic diversity of the Russian population of M. avium. A total of 85 M. avium subsp. hominissuis (MAH) clinical strains were isolated from patients (including 30 HIV-positive individuals) with mycobacteriosis in St. Petersburg, 2008–2011. The identification of the microorganisms was carried out using biochemical tests and the PCR detection of the mobile elements IS901 and IS900, as well as of the polymorphism of restriction fragments of the hsp65 gene. The genetic diversity of the isolates was evaluated by VNTR typing based on eight variable-number tandem repeats (VNTRs) (292, X3, 25, 47, 3, 7, 10, and 32 [Thibault et al., 2007]). The MAH population studied was characterized by 15 VNTR types, including nine unique patterns and six clusters of isolates with identical eight-digit profiles. The largest clusters (22221128 and 24221128) included 45 (59.2%) and 15 (19.7%) isolates, respectively; the others contained 2–7 strains. The strains of the cluster 2533112’8 possessed a truncated TR10 locus (allele 2′). Taking into account the absence of the epidemiological links between the patients and the fact that the infection was presumably delivered from the environment, the high rate of clustering of MAH isolates can be explained by the low discriminatory power of the eight-locus VNTR-typing scheme (HGDI 0–0.61).     

Glucose Metabolism in Healthy Subjects and in Patients with Carbohydrate and Lipid Metabolic Disorders

The rate of glucose oxidation was studied by measurement of the ¹³C concentration in expired air with simultaneous detection of the activity of the pyruvate dehydrogenase complex in subjects with obesity and patients with type II diabetes. Intake of small amounts of glucose did not change the rate of glucose oxidation in subjects with obesity as compared to healthy controls. However, intake of large amounts of glucose resulted in a considerable increase in the rate of glucose oxidation without a hypoxic shift. In patients with diabetes mellitus, the rate of glucose oxidation decreased with increasing tissue hypoxia.